Calcific aortic stenosis is a common cause of acquired valvular heart disease with substantial morbidity and mortality. Its incidence increases exponentially in older patient populations. Fibrosis, degeneration and subsequent calcification are no longer believed to be passive or purely degenerative in nature, but in fact are predominantly active processes mediated by underlying cellular mechanisms. Over time, as fibrosis and calcification worsens, valve leaflets become increasingly rigid, restricting their ability to open. This, in turn, impedes the antegrade flow of blood through the heart resulting in several clinical syndromes including progressive heart failure. Other causes of deformed and stenotic aortic valvular lesions include rheumatic heart disease, as well as nonacquired (i.e. congenital) heart disease. Initial stages of stenotic valvular heart conditions are well tolerated by the patient, but when leaflet restriction becomes severe, invasive measures such as aortic valve replacement have commonly been required.
With the advent of catheter-based cardiovascular procedures, minimally invasive balloon valvuloplasty techniques were developed to dilate stenosed valves, such as calcific, rheumatic and congenitally stenosed leaflets. During this procedure, a catheter having a deflated balloon is percutaneously inserted into a vein or artery and advanced until the balloon is positioned within the heart valve needing treatment. The balloon is then inflated to dilate the diseased valve opening, disrupting the rigid sheets of calcium and thereby permitting enhanced leaflet mobility. Balloon dilation, depending on the disease process, may result not only in the development of numerous flexible hinge points within fibrosed and calcified leaflets, but also separation of fused commissures. After the leaflets have been dilated, the balloon is deflated and removed from the patient's cardiovascular system.
Ideally, an infinite number of “hinge pointes” should be created circumferentially along the inner margin of the aortic valve annulus, from which the rigidly calcified leaflets arise. Retention of inflexible calcified ledges extending into the valve leaflets can prevent symmetric expansion and incomplete apposition of implanted stent valves against the annulus. This, in turn, may result in both peri and central valvular insufficiency of an inadequately deployed percutaneous stent-valve. Aggressive attempts to predilate with an oversized balloon can be complicated by an annular tear or rupture, resulting in potentially catastrophic and generally fatal complications. Predilatation with undersized balloons may avoid this complication but render the valve ill prepared for treatment.
In many current instances, valvuloplasty is performed with polymeric balloon catheters that can achieve relatively high pressures at a fixed diameter. Balloons made of non-distensible plastic materials are expanded using fluid pressure up to a certain diameter after which, increases in fluid pressure within the balloon produce very little change in balloon diameter. These balloons can achieve high pressures for an effective therapy, but have several inherent limitations.
For example, it is difficult to expand these balloons, and then return them to their pre-expansion configuration. The pre-expansion profile of these balloons can be somewhat reduced by prefolding during the manufacturing process. However, once inflated, the folded balloon segments are expanded within the vascular system. When deflated for removal, these segments arrange to a flattened state with a much larger profile, often called “winging”. Withdrawal of these balloons therefore requires larger vascular introductory sheaths and thereby increases the risk of trauma to the vessels, resulting in compromised blood flow to an extremity or post operative bleeding. Additionally, non-distensible balloons also have thick cones—transitions from the cylindrical diameter to the catheter shaft diameter. These regions of the balloon make the catheter stiff, thereby increasing the risk of vascular trauma and increasing the difficulty of advancing through tortuous peripheral arterial anatomy.
Since the radial dimensions of the catheter balloon must greatly increase when inflated to achieve aortic valve dilation, a highly elastic material such as latex can be used to construct the balloon. Distensible balloons use these elastic materials and generally have excellent initial profiles and improved flexibility for introduction and travel through the vascular system. In addition, they possess good deflated profiles for removal from the vascular system. However, these highly elastic materials have significant limitations. For example, it may be difficult to control the expansion diameter of these balloons. The elastic materials continue to expand in diameter as pressure increases and therefore have no inherent limit on maximal diameter as with non-distensible balloons. Thus, distensible balloons can be unsafe for valvuloplasty, as the elastic limit can easily be exceeded when the balloon is fully inflated, potentially causing the balloon to rupture within the patient. Additionally, the balloon diameters can become too large for the valve being dilated causing rupture and tearing of both the valve and its adjacent structures.
In addition, prior art catheter balloons have been associated with mechanical injury to the cardiac chambers. For example, tissue near the ventricular apex may be injured due to the forceful longitudinal movement of the inflated balloon across the valve and within the cardiac chamber. In another example, sudden and unexpected movements of the balloon can cause further tissue damage. Blood and the vascular wall surface are inherently slippery against common catheter balloons which can result in significant balloon migration. As inflation fluid (e.g., contrast media) is introduced, the catheter balloon enlarges and eventually assumes a cylindrical or axial ovoid shape. This shape creates a tendency for the balloon to suddenly and uncontrollably pop in and out of the valve site and migrate deep into the left ventricle. In some situations, this sudden balloon movement following inflation can increase the difficulty to position the balloon accurately within the valve leaflets, cause tissue damage and even catastrophic puncturing of the left ventricle.
Further, typical catheter balloon shapes tend to completely obstruct the flow of blood through the heart while inflated. Without perfusion through or around the catheter, the catheter balloon inflation time is believe to be limited to a few seconds before risking complications due to profound hypotension.
A further disadvantage of prior art valvuloplasty balloons is its frequent failure to restore adequate flexibility to the aortic valve leaflets. That is, mere dilation with these previous balloon designs may not be enough to adequately open the severely fibrosed and calcified leaflets. The prior art balloon catheters are cylindrical in shape when fully inflated and thus have their maximal inflated diameter limited by the narrower sinotubular ridge and valve annulus at the distal and proximal margins respectively of the aortic root sinuses. Efforts to expand beyond these limits can result in tearing of the aortic valve annulus, catastrophic aortic insufficiency or rupture of the aortic root. In addition, traditional balloon catheter methods generally result in eventual restenosis of the aortic valve leaflets in 6-18 months, negating some or all of the regained flexibility.
Examples of some of these prior art catheter designs, as well as other related catheter designs are discussed and disclosed in the following U.S. Pat. Nos. 4,327,736; 4,777,951; 4,787,388; 4,878,495; 4,819,751; 4,909,252; 4,986,830; 5,352,199; and 5,947,924 and U.S. Pat. Publication No. 2005/0090846; the contents of all of which are incorporated by reference.
What is needed is a balloon valvuloplasty catheter that overcomes all of these disadvantages of the prior art. Indeed, what is needed is an invention that not only overcomes the disadvantages of the prior art in treating calcific aortic stenosis but also aortic stenosis resulting from congenitally abnormal valves and/or rheumatically injured valves.